ArticleCNS neuroscience & therapeutics2024
BRCC3 mediates inflammation and pyroptosis in cerebral ischemia/reperfusion injury by activating the NLRP6 inflammasome.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- PI3K-Akt signaling network crosstalk in cerebral ischemia/reperfusion injury: Mechanisms and therapeutic implications.Chinese medical journal · 2026Review
- Naoluotong granules inhibit necroptosis of neural cells and improve cerebral ischemia-reperfusion injury by regulating the RIP1/NIK/IKKα/NF-κB pathway.Histology and histopathology · 2026Article
- The roles of microglia and astrocytes in inflammasomes and neurological disorders.Neural regeneration research · 2026Article
- LINC01094 exacerbates acute cerebral infarction by regulating miR-499a-5p.Metabolic brain disease · 2026Article
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- Phosphorylation of NLRP6 at Serine 27 site is critical for NLRP6 inflammasome activation and neurological impairment in ischemic stroke.Cell communication and signaling : CCS · 2026Article
- Deubiquitinating enzymes at the crossroads of blood-brain barrier integrity and neurodegeneration: mechanistic insights, therapeutic targeting and future directions.Tissue barriers · 2026Review
- Complexes Formed by the K63-Specific Deubiquitinating Enzyme BRCC36: New Promising Therapeutic Targets in Human Disease.Biomolecules · 2025Review
- Knockdown of USP22 alleviates LPS-induced microglial inflammation and mouse depressive-like behaviors via KAT2A.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Polygalasaponin F alleviates cerebral ischemia-reperfusion injury through inhibiting mitophagy.Metabolic brain disease · 2025Article
- Pyroptosis: inflammatory cell death mechanism and its pathological roles in neurological diseases and injuries.Apoptosis : an international journal on programmed cell death · 2025Review
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
- ncRNAs-Mediated Pyroptosis in Cerebral Ischemia-Reperfusion Injury: Pathophysiology, Mechanisms, and Therapeutic Perspectives.Current issues in molecular biology · 2025Review
- Necroptosis in vascular cognitive impairment: mechanisms and therapeutic potential.Frontiers in aging neuroscience · 2025Review
- Anemoside B4 mitigates endoplasmic reticulum stress-induced apoptosis post cerebral ischemia/reperfusion injury in rats.Iranian journal of basic medical sciences · 2025Article
- Research progress of deubiquitinating enzymes in cerebral ischemia-reperfusion injury.Frontiers in aging neuroscience · 2025Review
- BRCC3 mediates inflammation and pyroptosis in cerebral ischemia/reperfusion injury by activating the NLRP6 inflammasome.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
aimsNeuroinflammation and pyroptosis are key mediators of cerebral ischemia/reperfusion (I/R) injury-induced pathogenic cascades. BRCC3, the human homolog of BRCC36, is implicated in neurological disorders and plays a crucial role in neuroinflammation and pyroptosis. However, its effects and potential mechanisms in cerebral I/R injury in mice are unclear.
methodsCellular localization of BRCC3 and the interaction between BRCC3 and NLRP6 were assessed. Middle cerebral artery occlusion/reperfusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R) models were established in mice and HT22 cells, respectively, to simulate cerebral I/R injury in vivo and in vitro.
resultsBRCC3 protein expression peaked 24 h after MCAO and OGD/R. BRCC3 knockdown reduced the inflammation and pyroptosis caused by cerebral I/R injury and ameliorated neurological deficits in mice after MCAO. The effects of BRCC3 on inflammation and pyroptosis may be mediated by NLRP6 inflammasome activation. Moreover, both BRCC3 and its N- and C-terminals interacted with NLRP6, and both BRCC3 and its terminals reduced NLRP6 ubiquitination. Additionally, BRCC3 affected the interaction between NLRP6 and ASC, which may be related to inflammasome activation.
conclusionBRCC3 shows promise as a novel target to enhance neurological recovery and attenuate the inflammatory responses and pyroptosis caused by NLRP6 activation in cerebral I/R injury.
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